Chrysin Suppressed Inflammatory Responses and the Inducible Nitric Oxide Synthase Pathway after Spinal Cord Injury in Rats

被引:69
|
作者
Jiang, Yong [1 ]
Gong, Fu-Liang [1 ]
Zhao, Guang-Ben [1 ]
Li, Jie [1 ]
机构
[1] Dalian Med Univ, Dept Orthoped, Affiliated Hosp 1, Dalian 116011, Peoples R China
来源
关键词
chrysin; spinal cord injury; neuroprotection; inflammation; inducible nitric oxide synthase; APOPTOSIS; CONTUSION; DEFICITS; NEURONS; DAMAGE; MODEL; INOS;
D O I
10.3390/ijms150712270
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chrysin (CH), a natural plant flavonoid, has shown a variety of beneficial effects. Our present study was conducted to evaluate the therapeutic potential of CH three days after spinal cord injury (SCI) in rats and to probe the underlying neuroprotective mechanisms. SCI was induced using the modified weight-drop method in Wistar rats. Then, they were treated with saline or CH by doses of 30 and 100 mg/kg for 26 days. Neuronal function was assessed with the Basso Beattle Bresnahan locomotor rating scale (BBB). The water content of spinal cord was determined after traumatic SCI. The NF-kappa B p65 unit, TNF-alpha, IL-1 beta and IL-6 in serums, as well as the apoptotic marker, caspase-3, of spinal cord tissues were measured using commercial kits. The protein level and activity of inducible nitric oxide synthase (iNOS) were detected by western blot and a commercial kit, respectively. NO (nitric oxide) production was evaluated by the determination of nitrite concentration. The rats with SCI showed marked reductions in BBB scores, coupled with increases in the water content of spinal cord, the NF-kappa B p65 unit, TNF-alpha, IL-1 beta, IL-6, iNOS, NO production and caspase-3. However, a CH supplement dramatically promoted the recovery of neuronal function and suppressed the inflammatory factors, as well as the iNOS pathway in rats with SCI. Our findings disclose that CH improved neural function after SCI in rats, which might be linked with suppressing inflammation and the iNOS pathway.
引用
收藏
页码:12270 / 12279
页数:10
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